Organ Fibrosis

Organ fibrosis is a pathological process characterized by excessive accumulation of extracellular matrix (ECM) proteins, leading to tissue scarring and hardening. The incidence of organ fibrosis is on the rise, driven by factors such as aging populations, increased rates of metabolic disorders, and chronic infections. In general, organ fibrosis and the resulting organ failure are estimated to be responsible for at least a third of all disease-related deaths worldwide. In addition to being a major social burden, organ fibrosis also represents an immense economic cost to healthcare systems. Despite its widespread impact, effective treatments for organ fibrosis remain limited, with current therapies primarily focused on slowing disease progression rather than reversing fibrosis. This highlights the urgent need for novel therapeutic strategies that can address the underlying mechanisms of fibrosis and improve patient outcomes.

Idiopathic Pulmonary Fibrosis

Pulmonary fibrosis, including idiopathic pulmonary fibrosis (IPF), is a progressive disease that leads to severe loss of lung function, impaired quality of life, and often poor survival prognosis. IPF is a rare and chronic lung disease characterized by progressive scarring of the lung’s supporting tissue. This loss of lung function results in worsening symptoms such as persistent cough and breathlessness, severely impacting patients’ physical and emotional well-being.

IPF predominantly affects adults aged 65 to 70 and is more common in men, with risk factors including smoking, occupational dust exposure, and genetic predisposition. An estimated 3 million people were living with IPF globally in 2017, a number that continues to rise due to aging populations and improved diagnostic awareness.

Despite recent therapeutic advancements, IPF treatments primarily focus on slowing disease progression rather than reversing it. Left untreated, median survival is just 2-3 years. As a result, the disease imposes a considerable burden on patients and healthcare systems.

Liver Fibrosis

Chronic liver diseases represent a major global health burden, causing approximately 2 million deaths annually worldwide. It arises from various underlying causes, including viral infections (hepatitis B and C), alcohol-related liver disease, metabolic dysfunction-associated steatohepatitis (MASH), as well as autoimmune and genetic disorders. A key feature of chronic liver disease is the development of liver fibrosis, marked by the progressive accumulation of scar tissue that disrupts the normal architecture of the liver, impairs liver function, and significantly increases the risk of liver cancer. Furthermore, liver fibrosis leads to chronic portal hypertension, a major contributor to clinical complications such as fluid accumulation, internal bleeding, and hepatic encephalopathy. Its most advanced form, liver cirrhosis, ranks as the 11th leading cause of death globally.

Given the intricate and multifaceted nature of liver fibrosis, developing effective therapies remains a significant challenge. Current treatment options are limited, and successfully reversing fibrosis requires novel approaches that can target multiple aspects of the disease simultaneously.

Kidney Fibrosis

Chronic kidney disease (CKD) affects more than 10% of the world’s population, with kidney fibrosis representing the final pathway of disease progression. Kidney fibrosis is a complex progressive condition characterized by excessive accumulation of extracellular matrix (ECM) components, leading to the scarring and hardening of kidney tissue. Ongoing injury and inflammation in CKD trigger myofibroblast activation and proliferation, the cells that produce collagen and other ECM proteins underlying fibrosis. This process creates a self-perpetuating cycle of injury, inflammation, and fibrosis that ultimately leads to irreversible loss of kidney function, highlighting the critical need for targeted therapies that can interrupt this process and prevent or reverse disease progression.